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Re: Amatuer17 post# 104287

Monday, 05/25/2015 12:39:09 PM

Monday, May 25, 2015 12:39:09 PM

Post# of 403579
I am assuming that K activates the defective p53 gene only if its present in clinical concentrations.

This is not gene therapy which is the cornerstone of companies like bluebird which are actually inserting the defective gene via a viral vector or the patients own stem cells.

For K to work it must be present in the plasma and delivered to the defective cancer cells.

I am hoping that the mechanism of action of K includes apoptosis of the cancer cells with cell cycle regeneration of native cells that have complete genetic copies of alleles that include native p53.

This all remains to be seen as phase 1 winds into phase 3.

the reason AML is of interest lies in the fact that one correction of the hematopoietic white blood cell precursor in the bone marrow may cure the AML within 6 to 7 cycles of K infusion.

This is because the lifespan of a white blood cell is about 35 days but lifelong for memory white cells found in the granulocytes in the bone marrow .

AML could be a treatable disease with K not different then hypertension can be treated with beta blockers or diuretics .....
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